Switch in brain could halt Alzheimer's

John Bingham

London: Scientists have found a potential way to stop the progression of Alzheimer's disease, raising the prospect of new treatments for the condition.

A team at Cambridge University, working with partners in Sweden and Estonia, has identified a molecule that can block Alzheimer's at a crucial stage in its development. It is the first time a means of breaking the cycle in the development of Alzheimer's has been identified.

Researchers believe the technique could also be used to identify other molecules which may be used as future treatments to curb the condition's growth. Alzheimer's charities on Monday described the development as exciting.

More than 520,000 people in Britain are estimated to be living with Alzheimer's, the most common cause of dementia. Dementia-related conditions are the biggest cause of death among women in Britain and are just behind heart disease and cancer for men.

Alzheimer's develops when proteins in the brain malfunction and stick together to become fibres. They in turn eventually form clusters that are toxic to nerve cells. The second stage of that process is believed to set off a chain reaction which multiplies the number of clusters, hastening the development of the most devastating effects.

Researchers at the Centre for Misfolding Diseases in Cambridge's Chemistry Department have identified that natural proteins called Brichos can stick to the fibres, preventing them merging with others to form the damaging clusters and therefore limiting the effects.

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They believe the method may also help them identify other so-called "chaperone molecules" which could attach themselves in a similar way, raising the prospect of a new generation of treatments.

Dr Ian Le Guillou, a research officer at the Alzheimer's Society, said: "While most current research attempts to break up these clumps or reduce their impact on brain cells, this new discovery identifies a molecule that reduces the rapid accumulation of the toxic clumps.

"This revelation is exciting as it gives scientists a whole new way of looking at the problem, opening the doors to possible new treatments."

Dr Samuel Cohen, a research fellow at St John's College in Cambridge and a lead author of a paper in the journal Nature Structural & Molecular Biology, said: "A great deal of work in this field has gone into understanding which microscopic processes are important in the development of Alzheimer's disease.

"Our study shows, for the first time, one of these critical processes being specifically inhibited, and reveals that by doing so we can prevent the toxic effects of protein aggregation that are associated with this terrible condition."

He said the breakthrough came after the researchers worked out how to model what might happen if one stage in the process of developing Alzheimer's was effectively "switched off" and then experimented with different molecules to see which might do this. They confirmed their findings with tests involving mice.

"It's striking that nature - through molecular chaperones - has evolved a similar approach to our own by focusing on very specifically inhibiting the key steps leading to Alzheimer's," he said.

Dr Laura Phipps, of Alzheimer's Research UK, said that "this technically challenging study has revealed clues to how to block one important chain of events in the disease" but further research is needed to determine its potential.